ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2025
M2 Macrophages are Major Mediators of Germline Risk of Endometriosis and Explain Pleiotropy With Comorbid Traits.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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Who cites it
6 citing papers in PubMed.
- Parabacteroides goldsteinii and its metabolite 7-KLCA attenuate endometriosis via TGR5 to reprogram macrophages by modulating the PPARγ/GPR132 axis.NPJ biofilms and microbiomes · 2026Article
- Is Recurrent Endometriosis a Reprogrammed Disease? Molecular Persistence Beyond Surgical Clearance.Cells · 2026Review
- Senescence-Driven Remodeling Defines an Aggressive and Immunomodulatory Subtype of Endometriosis.Aging cell · 2026Article
- Deciphering immune-inflammatory dysregulation in the endometriotic microenvironment: insights from single-cell omics and artificial intelligence.Frontiers in immunology · 2026Review
- M2 Macrophages are Major Mediators of Germline Risk of Endometriosis and Explain Pleiotropy With Comorbid Traits.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Pro-endometriosis macrophage release of IL-33 is key for endometriosis pain and lesion formation.bioRxiv : the preprint server for biology · 2025Article
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16 authors.
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Abstract
Endometriosis is a common gynecologic condition that causes chronic, life-altering symptoms including pain and infertility. There is an urgent need for new non-hormonal targeted therapeutics to treat endometriosis, but until very recently, the cellular and molecular signatures of endometriotic lesions are undefined, hindering the development of clinical advances. Integrating inherited risk data from analyses of >45 0000 individuals with ≈35 0000 single-cell transcriptomes from 21 patients, M2-macrophages as candidate drivers of disease susceptibility are uncovered, and nominating IL1 signaling as a central hub impacted by germline genetic variation associated with endometriosis risk. Extensive functional follow-up confirmed these associations and revealed a pleiotropic role for this pathway in endometriosis. Population-scale expression quantitative trait locus analysis demonstrates that genetic variation controlling IL1A expression is associated with endometriosis risk variants. Manipulation of IL1 signaling in state-of-the-art in vitro decidualized endometrial organoids impacts epithelial differentiation, and in an in vivo endometriosis model, treatment with anakinra (an interleukin-1 receptor antagonist) results in a significant, dose-dependent reduction in spontaneous and evoked pain and dampened pro-angiogenic signaling. Together, these studies highlight non-diagnostic cell types as central to endometriosis susceptibility and support IL1 signaling as an important actionable pathway for this disease.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.